Further supporting the clinical translational potential for USP10 inhibition in patients with CML, we observed that the protein levels of both USP10 and SKP2 in these patients were significantly increased (Fig. 7a–c) and primary monocytes from CML patients were more sensitive to the treatment of Spautin-1, compared with those from normal volunteers (Fig. 7d). The gene discussed is USP10; the disease is chronic myelogenous leukemia, BCR-ABL1 positive.